MacDermott A B, Connor E A, Dionne V E, Parsons R L
J Gen Physiol. 1980 Jan;75(1):39-60. doi: 10.1085/jgp.75.1.39.
Excitatory postsynaptic currents (EPSCs) have been studied in voltage-clamped bullfrog sympathetic ganglion B cells. The EPSC was small, rose to a peak within 1-3 ms, and then decayed exponentially over most of its time-course. For 36 cells at --50 mV (21-23 degrees C), peak EPSC size was --6.5 +/- 3.5 nA (mean +/- SD), and the mean decay time constant tau was 5.3 +/- 0.9 ms. tau showed a small negative voltage dependence, which appeared independent of temperature, over the range --90 to --30 mV; the coefficient of voltage dependence was --0.0039 +/-0.0014 mV-1 (n = 29). The peak current-voltage relationship was linear between --120 and --30 mV but often deviated from linearity at more positive potentials. The reversal potential determined by interpolation was approximately --5 mV. EPSC decay tau had a Q10 = 3. The commonly used cholinesterase inhibitors, neostigmine and physostigmine, exhibited complex actions at the ganglia. Neostigmine (1 X 10(-5)M) produced a time-dependent slowing of EPSC decay without consistent change in EPSC size. In addition, the decay phase often deviated from a single exponential function, although it retained its negative voltage dependence. With 1 x 10(-6) M physostigmine, EPSC decay was slowed by the decay phase remained exponential. At higher concentrations of physostigmine, EPSC decay was markedly prolonged and was composed of at least two decay components. High concentrations of atropine (10(-5) to 10(-4) M) produced complex alterations in EPSC decay, creating two or more exponential components; one decay component was faster and the other was slower than that observed in untreated cells. These results suggest that the time-course of ganglionic EPSC decay is primarily determined by the kinetics of the receptor-channel complex rather than hydrolysis or diffusion of transmitter away from the postsynaptic receptors.
在电压钳制的牛蛙交感神经节B细胞中对兴奋性突触后电流（EPSC）进行了研究。EPSC较小，在1 - 3毫秒内升至峰值，然后在其大部分时间进程中呈指数衰减。对于36个处于-50毫伏（21 - 23摄氏度）的细胞，EPSC峰值大小为-6.5±3.5纳安（平均值±标准差），平均衰减时间常数τ为5.3±0.9毫秒。在-90至-30毫伏范围内，τ呈现出较小的负电压依赖性，且似乎与温度无关；电压依赖性系数为-0.0039±0.0014毫伏⁻¹（n = 29）。在-120至-30毫伏之间，峰值电流-电压关系呈线性，但在更正的电位时常常偏离线性。通过插值法确定的反转电位约为-5毫伏。EPSC衰减τ的Q10 = 3。常用的胆碱酯酶抑制剂新斯的明和毒扁豆碱在神经节表现出复杂的作用。新斯的明（1×10⁻⁵摩尔/升）使EPSC衰减出现时间依赖性减慢，而EPSC大小无一致变化。此外，衰减相常常偏离单一指数函数，尽管仍保持其负电压依赖性。使用1×10⁻⁶摩尔/升毒扁豆碱时，EPSC衰减减慢且衰减相仍为指数形式。在更高浓度的毒扁豆碱作用下，EPSC衰减明显延长且由至少两个衰减成分组成。高浓度阿托品（10⁻⁵至10⁻⁴摩尔/升）使EPSC衰减发生复杂改变，产生两个或更多指数成分；一个衰减成分比未处理细胞中观察到的更快，另一个则更慢。这些结果表明，神经节EPSC衰减的时间进程主要由受体-通道复合物的动力学决定，而非递质从突触后受体的水解或扩散。
